O'Rear J J, Mizutani S, Hoffman G, Fiandt M, Temin H M
Cell. 1980 Jun;20(2):423-30. doi: 10.1016/0092-8674(80)90628-5.
Ten clones of Charon 4A containing proviruses of spleen necrosis virus, an avian retrovirus, and flanking chicken DNA sequences were isolated and characterized. Some clones gave rise to progeny with viral DNA sequences deleted or duplicated, probably as a result of crossing-over in the 600 bp terminal redundancy in viral DNA. The cellular sequences are different in each clone, indicating that all the proviruses are integrated in different sites in cellular DNA. Six clones are infectious and four are not. All the infectious molecules containing a provirus are of a similar size and are smaller than the noninfectious molecules containing a provirus. The viral DNA is not apparently different in eight clones, but two clones, one infectious and one noninfectious, lack two restriction sites each. Large changes in proviral DNA therefore do not seem responsible for the lack of infectivity of some clones. These results are consistent with the hypothesis that neighboring cellular DNA sequences control proviral expression (infectivity).
分离并鉴定了10个含有脾脏坏死病毒(一种禽逆转录病毒)前病毒及侧翼鸡DNA序列的Charon 4A克隆。一些克隆产生了病毒DNA序列缺失或重复的后代,这可能是病毒DNA中600 bp末端冗余发生交叉的结果。每个克隆中的细胞序列都不同,这表明所有前病毒都整合在细胞DNA的不同位点。6个克隆具有感染性,4个没有。所有含有前病毒的感染性分子大小相似,且比含有前病毒的非感染性分子小。8个克隆中的病毒DNA显然没有差异,但有两个克隆,一个有感染性,一个没有感染性,各自缺少两个限制酶切位点。因此,前病毒DNA的巨大变化似乎并非某些克隆缺乏感染性的原因。这些结果与邻近细胞DNA序列控制前病毒表达(感染性)的假说一致。